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By V. Topork. Medical College of Georgia.

Breastfeeding Thyroid hormone preparations and antithyroid medications are generally safe in breastfeeding women women 20mg levitra soft. Thyroid hormone preparations and antithyroid medications can be used successfully to treat thyroid dysfunction in the older adult 20 mg levitra soft. Radioactive Iodine Physical Properties 131 Iodine-131 ( I) is a radioactive isotope of stable iodine that emits a combination 131 of beta particles and gamma rays levitra soft 20mg. Hence levitra soft 20 mg, after 56 days (seven half-lives) , less than 1% of 131 the radioactivity in a dose of I remains . Use in Graves Disease 131 I can be used to destroy thyroid tissue in patients with hyperthyroidism . The objective is to produce clinical remission without causing complete destruction of the gland . Unfortunately , delayed hypothyroidism , due to excessive thyroid damage, is a frequent complication. Effect on the Thyroid 131 Like stable iodine, I is concentrated in the thyroid gland. Destruction of thyroid tissue is produced primarily by emission of beta particles. About 66% of 131 patients with Graves disease are cured with a single exposure to I. First, the effect of treatment is delayed, taking several months to become maximal. Second, and more important, treatment is associated with a significant incidence of delayed hypothyroidism. Hypothyroidism results from excessive dosage and occurs in up 131 to 90% of patients within the first year after I exposure. Who Should Be Treated and Who Should Not 131 I is indicated for adults with hyperthyroidism, as well as patients who have not responded adequately to antithyroid drugs or to subtotal thyroidectomy. Also, there is 131 concern that administration of I to young patients may carry a slight risk for 131 cancer. It should be noted, however, that there is no evidence that the use of I in Graves disease has ever caused cancer of the thyroid or any other tissue. Exposure of the fetus to I after the first trimester may damage the immature thyroid, and exposure to radiation at any point in fetal life carries a risk for generalized developmental 131 harm. Dosage 131 Dosage of I is determined by thyroid size and by the rate of thyroidal iodine uptake. However, because most forms of thyroid cancer do not accumulate iodine, only a small percentage of patients 131 are candidates for I therapy. Because high amounts of radioactivity are involved, body wastes must be disposed of properly. Diagnostic Use 131 I is employed to diagnose a variety of thyroid disorders, including 131 hyperthyroidism, hypothyroidism, and goiter. After I administration, the 131 thyroid is scanned for uptake of radioactivity; the amount and location of I uptake reveal the extent of thyroid activity. Doses for diagnosis are minuscule (less than 1 microcurie for children and less than 10 microcuries for adults). Please note that, although 131 123 I can be used for diagnosis, the preferred isotope is I. Nonradioactive Iodine: Lugol Solution Description Lugol solution, also known as strong iodine solution, is a mixture containing 5% elemental iodine and 10% potassium iodide. Mechanism of Action When present in high concentrations, iodide has a paradoxical suppressant effect on the thyroid. Second, high concentrations of iodide inhibit thyroid hormone synthesis by suppressing both the iodination of tyrosine and the coupling of iodinated tyrosine residues. Third, high concentrations of iodine inhibit release of thyroid hormone into the blood. Therapeutic Use Strong iodine solution can be given to hyperthyroid individuals to suppress thyroid function in preparation for thyroidectomy. In most cases, plasma levels of thyroid hormone are reduced with methimazole before initiating strong iodine solution. In addition to its use before thyroidectomy, strong iodine solution is employed in thyrotoxic crisis. Signs and symptoms include a brassy taste, a burning sensation in the mouth and throat, soreness of the teeth and gums, frontal headache, coryza (nasal inflammation and sneezing), salivation, and various skin eruptions. Treatment consists of gastric lavage (to remove iodine from the stomach) and giving sodium thiosulfate (to reduce iodine to iodide). Dosage and Administration When employed to prepare hyperthyroid patients for thyroidectomy, strong iodine solution is administered in a dosage of 5 to 7 drops 3 times daily for 10 days immediately preceding surgery. Iodine solution should be mixed with juice or some other beverage to mask its unpleasant taste. Beta Blockers Propranolol and other beta blockers can suppress tachycardia and other symptoms of Graves disease. Benefits derive from beta-adrenergic blockade, not from reducing levels of T or T. We begin this chapter with a discussion of how estrogens and progestins regulate physiologic processes. Estrogens and progestins (also known as progestogens) are hormones with multiple actions. They promote female maturation and help regulate the ongoing activity of female reproductive organs. In addition, small amounts of estrogens and progestins are produced in peripheral tissues. The Menstrual Cycle Because much of the clinical pharmacology of the estrogens and progestins is related to their actions during the menstrual cycle, understanding the menstrual cycle is central to understanding these hormones. The anatomic and hormonal changes that take place during the cycle are shown in Fig. As indicated, the first half of the cycle (days 1 through 14) is called the follicular phase, and the second half is called the luteal phase. Ovarian and Uterine Events The menstrual cycle consists of a coordinated series of ovarian and uterine events. In the ovary, the following sequence occurs: (1) several ovarian follicles ripen; (2) one of the ripe follicles ruptures, causing ovulation; (3) the ruptured follicle evolves into a corpus luteum; and (4) if fertilization does not occur, the corpus luteum atrophies. As these ovarian events are taking place, parallel events take place in the uterus: (1) while ovarian follicles ripen, the endometrium prepares for nidation (implantation of a fertilized ovum) by increasing in thickness and vascularity; (2) after ovulation, the uterus continues its preparation by increasing secretory activity; and (3) if implantation fails to occur, the thickened endometrium breaks down, causing menstruation, and the cycle begins anew. The Roles of Estrogens and Progesterone The uterine changes that occur during the cycle are brought about under the influence of estrogens and progesterone produced by the ovaries. During the first half of the cycle, estrogens are secreted by the maturing ovarian follicles. At midcycle, one of the ovarian follicles ruptures and then evolves into a corpus luteum. For most of the second half of the cycle, estrogens and progesterone are produced by the newly formed corpus luteum. At the end of the cycle, the corpus luteum atrophies, causing production of estrogens and progesterone to decline. In response to the diminished supply of ovarian hormones, the endometrium breaks down. Precisely timed alterations in the secretion of these hormones are responsible for coordinating the structural and secretory changes that occur throughout the menstrual cycle. Estrogens Biosynthesis and Elimination Females In premenopausal women, the ovary is the principal source of estrogen. During the follicular phase of the menstrual cycle, estrogens are synthesized by ovarian follicles; during the luteal phase, estrogens are synthesized by the corpus luteum. In the periphery, some of the estradiol secreted by the ovaries is converted into estrone and estriol, hormones that are less potent than estradiol itself. Estrogens are eliminated by a combination of hepatic metabolism and urinary excretion. In the human male, small amounts of testosterone are converted into estradiol and estrone by the testes. Activating these surface receptors produces a rapid response—more rapid than can be produced by activating nuclear receptors. Physiologic and Pharmacologic Effects Effects on Primary and Secondary Sex Characteristics of Females Estrogens support the development and maintenance of the female reproductive tract and secondary sex characteristics. These hormones are required for the growth and maturation of the uterus, vagina, fallopian tubes, and breasts. Estrogens have a profound influence on physiologic processes related to reproduction. During the follicular phase of the menstrual cycle, estrogens promote (1) ductal growth in the breast, (2) thickening and cornification of the vaginal epithelium, (3) proliferation of the uterine epithelium, and (4) copious secretion of thickened mucus from endocervical glands. In addition, estrogens increase vaginal acidity (by promoting local deposition of glycogen, which is then acted on by lactobacilli and corynebacteria to produce lactic acid). At the end of the menstrual cycle, a decline in estrogen levels can bring on menstruation. However, it is the fall in progesterone levels at the end of the cycle that normally causes breakdown of the endometrium and resultant menstrual bleeding. However, final transformation of the breast for milk production requires the combined influence of estrogen, progesterone, and human placental lactogen. Under normal conditions, bone undergoes continuous remodeling, a process in which bone mineral is resorbed and deposited in equal amounts. The principal effect of estrogens on the process is to block bone resorption, although estrogens may also promote mineral deposition. During puberty, the long bones grow rapidly under the combined influence of growth hormone, adrenal androgens, and low levels of ovarian estrogens. When estrogen levels grow high enough, they promote epiphyseal closure and thereby bring linear growth to a stop. Cardiovascular Effects Cardiovascular disease is much less common in premenopausal women. For example, estrogen receptors in the vascular smooth muscle respond to activation by decreasing vasoconstriction. Activation of estrogen receptors in vessel endothelium results in the production of nitric oxide, which results in vasodilation and increased perfusion. Estrogens suppress coagulation by increasing the activity of factors that promote breakdown of fibrin, a protein that reinforces blood clots. The net effect—increased or decreased coagulation—may be determined by a hereditary defect in one of these targets. They also have a role in neuronal growth and repair through stimulation of nerve growth factors. Estrogen-induced synaptic changes, coupled with estrogen-promoted increases in synaptic serotonin, dopamine, and norepinephrine, are thought to preserve cognitive function, enhance short-term memory, and regulate mood. Cerebral perfusion is also enhanced by the release of nitric acid and the resulting vasodilation. In conditions that lead to insulin resistance due to impaired transport, estrogen has been shown to increase insulin sensitivity to promote glucose uptake. Estrogens also have a role in insulin secretion and are believed to protect pancreatic islet beta cells from certain types of injury. Physiologic Alterations Accompanying Menopause Menopause may occur as the result of surgery (i. Natural menopause typically begins at about age 51 to 52 years, with 95% of women entering menopause between the ages of 45 and 55 years. During the initial phase, the menstrual cycle becomes irregular, anovulatory cycles may occur, and periods of amenorrhea may alternate with menses. Production of ovarian estrogens decreases gradually, coming to a complete stop several years after menstruation has ceased. Prominent symptoms experienced by the patient include vasomotor symptoms, sleep disturbances, and urogenital atrophy. Vasomotor Symptoms Vasomotor symptoms (hot flashes and night sweats) develop in about 70% of postmenopausal women. Episodes are characterized by sudden skin flushing, sweating, and a sensation of uncomfortable warmth. In most women, hot flashes abate within several months to a few years; in others, they may persist for a decade or more. Urogenital Atrophy Of all structures in the body, the urethra and vagina have the highest concentrations of estrogen receptors. Activation of these receptors maintains the functional integrity of the urethra and vaginal epithelium. Hence, when estrogen levels decline during menopause, these structures undergo degenerative change. In addition, alterations in vaginal secretions result in decreased acidity, which can allow the growth of pathogenic bacteria, resulting in vaginal infections. Mental Changes Many women report cognitive changes such as difficulty in problem solving and short-term memory loss around the time when menopause begins. These, also, tended to occur during the time of transition and often compounded sleep disturbances. Bone Loss In the absence of estrogen, bone resorption accelerates, leading to a 12% loss of bone density shortly after menopause. Osteoporosis is characterized by bone demineralization, altered bone architecture, and reduced bone strength. Compression fractures of the vertebrae are common and can decrease height and produce a hump. In osteoporotic women, fractures of the hip and wrist can result from minimal trauma. These are thought to have a role in the increase in cardiovascular disease that increases after menopause. Menopausal Hormone Therapy Hormone therapy in postmenopausal women is the most common noncontraceptive use of estrogens.

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Her normal growth points away from inflam- matory bowel disease 20 mg levitra soft, so invasive procedures and extensive laboratory testing are not required levitra soft 20mg. With no other symptoms and a normal white count levitra soft 20 mg, reassurance and observation are appropriate management 20mg levitra soft. Signs and symptoms may include fever , tachycardia , leukocytosis , anemia , hypo- tension , colonic dilation on radiography , dehydration, electrolyte abnormal- ity, and altered mental status. Her recent use of clindamycin makes pseudomembranous (ie, Clostridium difficile) colitis more likely. Irritable bowel syndrome is a relatively benign condition and would not have these radiographic findings. Salmonella typhi can cause toxic colitis, but without a travel or exposure history, this is less likely. This child probably has celiac disease, an immune-mediated inflammation of the small intestine in response to dietary gluten. The symptoms in this patient began when additional items were added to the diet around 6 months of age. Commercial formulas are typically gluten free, so symptoms will typi- cally appear between 6 and 24 months of age once parents introduce gluten- containing foods. While presentation in childhood is “classic,” many children and adults will first present at an older age, some with constipation, with bulky and foul-smelling stools. Antibody screening has become quite reliable, but diagnosis requires a duodenal biopsy, and must be done while the child is on a gluten-containing diet. The most common causes of rectal bleeding in the infant period are a milk protein allergy and an anal fissure. The patient in the case presenta- tion has no physical examination finding, so milk protein allergy is more likely. However, with a normal physical examination and no emesis, this diagnosis is unlikely. The abdominal pain is periumbilical, started 12 hours prior, is 9 out of 10 on the pain scale, and is constant, dull, and achy in nature. The acetaminophen her mother gave her did not reduce the pain, but is diminished only by lying supine. She is not hungry and has had one episode of nonbilious emesis 2 hours after the onset of the pain and one small, loose bowel movement. She denies dysuria, urinary frequency, and her last menses a week ago was normal; she denies having any sexual contact. On examination, she appears uncomfortable, has a heart rate of 110 beats/min, and a temperature of 100°F (37°C). Her abdominal examination reveals hypoactive bowel sounds, right rectus abdominis muscle rigidity, and tenderness to palpation, particularly in the periumbilical region. Her pelvic examination shows neither vaginal discharge nor cervical motion tenderness, but she has some abdomi- nal tenderness with gentle bimanual palpation. She has pain at the right lower quadrant when she flexes the right thigh and extends the hip to place her leg into the stirrup for the bimanual examination. She has no dysuria or sexual activity, and the pain appears unrelated to her menses. Her physical examination shows a quiet, rigid, tender abdomen, and positive psoas sign. Despite this adolescent’s denial of sexual activity, a urine pregnancy test should always be obtained in postmenarchal females. Considerations The definitive diagnosis of appendicitis is made once the pathologist finds inflam- mation histologically on the appendix specimen obtained by surgical removal. For this patient, the initial periumbilical abdominal pain followed by anorexia and vomit- ing suggests appendicitis. The pain of appendicitis classically begins periumbilically and then migrates to the right lower quadrant with maximal discomfort at McBurney point. However, the pain can occur laterally if the appendix is retrocecal or it can become diffuse if perforation occurs. If a patient presents early in the disease process, is lacking the characteristic physical examination findings, has inconclusive imaging findings, and thus has a questionable diagnosis, the child may be observed and undergo serial abdominal examinations for a few hours. However, once appendicitis seems likely, surgical management should occur in a timely fashion; perforation rates exceed 65% if diag- nosis is delayed beyond 36 to 48 hours from symptom onset. The most common complications of appendicitis are wound infection and intra-abdominal abscess or phlegmon formation, all of which occur more frequently with appendiceal perfora- tion. Other serious complications are sepsis, shock, ileus, peritonitis, and adhesions causing small bowel obstruction. A person’s life- time risk of appendicitis has been estimated at 6% to 20%, with the peak incidence in adolescence and a slight predilection for males. Appendicitis can develop via several mechanisms but a frequent cause is when the appendiceal lumen becomes obstructed, leading to vascular congestion followed by ischemia, gangrene, and ultimately perforation with spillage of contaminated material into the peritoneum. Obstruction can be caused intrinsically by inspissated fecal material (a fecalith) or by external compression from enlarged lymph nodes associated with bacterial or viral infections. A thorough history of the illness with close attention to symp- toms in other organ systems can help identify these causes; for example, subacute weight loss, sore throat, dysphagia, cough, jaundice, rash, vaginal discharge, and arthralgias do not typically occur with appendicitis. However, diarrhea can be present with appendicitis due to bowel inflammation or because enteric infection may have led to the initial appendiceal inflammation. Appendicitis usually begins with nonspecific symptoms of malaise and anorexia and then abdominal pain following in a few hours. Localization to the right lower quadrant may take 12 to 24 hours to appear, and pain will then be made worse with movement. Observation of the child getting on and off the examination table can be revealing; children with appendicitis avoid sudden movements. They may walk in a manner to decrease movement of the right side of the abdomen, such as a shuffle, refuse to hop off the table, or brace the abdomen against coughing. The abdomen is inspected, auscultated for bowel sounds, followed by gentle palpation for the area of maximal tenderness and rigidity. Gentle finger percussion is the best method to assess for peritoneal irritation (“rebound tenderness”). The utility of a rectal examination for children with suspected appendicitis is debatable so it is not routinely performed; it can, however, be helpful for localizing the pain source in a female adolescent. Thereafter, it would be expected to be greater than 10,000/mm3 and in cases of perforation, it may be greater than 20,000/mm3. Urinalysis is important to evaluate for glucose and large ketones or pyuria with nitrites and bacteria because these findings sug- gest diabetic ketoacidosis or urinary tract infection respectively. Mild hematuria or pyuria can occur with acute appendicitis because of irritation of the bladder or ure- teral wall. Psoas shadow obliteration, right lower quadrant intestinal dilation, scoliosis toward the affected region, and an appendicolith (seen in 10% of cases) support appendicitis. In a facil- ity experienced in using ultrasonography in children, ultrasound is the preferred imag- ing modality for a child suspected of having appendicitis. Its main limitation is that the appendix cannot always be visualized, which can occur if the appendix has already perforated, the patient is obese, or if there is a lot of bowel distention. If pelvic views are included, it can evaluate for ovarian pathology as the cause of the abdominal pain. Its disad- vantages are the amount of radiation exposure generated, increased cost, and it may give limited information without the use of contrast. Electrolyte abnormalities and volume depletion should be corrected preopera- tively as surgery within 48 hours from diagnosis does not influence perforation rate but reduces the risk of surgical complications. Analgesia should be given because it has been shown that it does not interfere with identifying the correct diagnosis. For perforated appendicitis, initial management consists of intravenous antibiotics and fluid replacement. Percutaneous catheters can be used to drain any abscess and then appendectomy is performed at a later time. Sickle cell disease (Case 13) may present as an abdominal pain crisis or with gall bladder disease. Pneumonia (Case 14) of the lower lobes is classically described as possibly causing abdominal pain similar to appendicitis. In the smaller child with significant lead poisoning (Case 25), abdominal pain along with achy joints, change in behavior, and encephalopathy can be seen. Bacterial enteritis (Case 28), especially when caused by Campylobacter or Yersinia sp. While malrotation (Case 34) typically occurs in smaller children, the presentation with abdominal pain may be similar; as part of the surgical procedure to correct a malrotation, an appendectomy typically is performed. Diabetic ketoacidosis (Case 42) presents in a vari- ety of ways, among which is abdominal pain; measurement of a serum sugar typically is performed as part of the evaluation of a patient with possible appendicitis. The patient with severe sore throat, abdominal pain, and fever may have streptococcal pharyngitis; the later complication of this condition is poststreptococcal glomerulonephritis (Case 52). Her mother says that she has also had poor appetite and two loose stools the day prior. Because of the pain, she is unable to sit up for lung auscultation or percussion of the costovertebral angles. For which of the following condi- tions would exclude appendicitis from the differential diagnosis? A urine dipstick on a clean-catch specimen shows 1+ leukocytes, trace blood, and trace ketones, but no nitrites and no bacteria. Send the patient immediately to the pediatric hospital for an abdominal ultrasound. Give him a prescription for trimethoprim-sulfamethoxazole; schedule a follow-up visit in 2 days to reevaluate the urine. Admit him to the hospital for intravenous antibiotics to treat presumed pyelonephritis. This child’s presentation is concerning for appendicitis, and she may have already perforated. Abdominal radiographs can be included in the evaluation of abdominal pain but is not the appropriate imaging tool when appendicitis is strongly suspected. It is not uncommon for appendicitis to cause stool changes, either obsti- pation or ileus from the inflammation. Diarrhea can occur by the same mechanism or may be part of the initial illness that created the appendici- tis. A negative pregnancy test only excludes ruptured ectopic pregnancy as her diagnosis. Scleral icterus and tender posterior cervical lymph nodes are not features of appendicitis. This boy’s symptoms and signs can be caused by appendicitis so prompt imaging to further confirm the diagnosis is indicated. His urinalysis is not consistent with a urinary tract infection, especially because he has peripheral leukocytosis; the urine abnormalities are most likely the result of bladder wall or ureter irritation caused by an inflamed appendix. Waiting to perform diagnostic imaging another 24 hours would increase the risk of perforation to 65% or more. Children with abdominal pain require a comprehensive examination but rectal examination is rarely indicated. Inspection of the oropharynx will show pharyngitis or tonsillitis and her age may prevent her from disclosing that she has pain in her throat. Auscultation and percussion of the abdomen should always be done when pain is reported. If you encounter the child supine on the examination table, it is important to watch the child go through changes in position, such as sitting up for the lung examination, transferring off the table, and then her gait. She first started feeling ill 10 days ago with general malaise, headache, and nau- sea. She has worsening sore throat and difficulty swallowing solid foods; she is drinking well. She takes an oral contraceptive daily and took two doses of ampicillin yesterday (left over from a prior illness). She has mild supraorbital edema, bilaterally enlarged tonsils that are coated with a shaggy gray exudate, a few petechiae on the palate and uvula, bilateral posterior cervical lymphadenopathy, and a spleen that is palpable 3 cm below the costal margin. Her examination reveals a fever, rash, tonsillar hypertrophy with exudate, posterior cer- vical lymphadenopathy, and splenomegaly. Differential diagnosis includes group A β-hemolytic streptococcal pharyngitis, but streptococcal infection typi- cally does not have a prodrome similar to this case or cause splenomegaly. Fever, posterior cervical adenopathy, and sore throat are seen in more than 80% of cases. The virus is excreted in saliva; infection results from mucosal contact with an infected individual or from contact with a contami- nated fomite. Affected patients usually have peripheral blood lym- phocytosis, composed in large measure of atypical lymphocytes. Physical findings during an acute infection may include generalized lymphadenopathy, splenomegaly, and tonsillar enlargement with exudate. Additional acute findings in small children include otitis media, abdominal pain, and diarrhea. Hepatomegaly and rash are seen more often in small children than in older individuals. The presence of heterophile antibodies (Monospot) is a useful diagnostic test in children older than 5 years; the results are unreliable in younger children. Other laboratory findings include a lymphocytic leukocytosis, with approxi- mately 20% to 40% atypical lymphocytes. Neurologic sequelae include Bell palsy, seizures, aseptic meningitis or encephalitis, Guillain-Barré syn- drome, optic neuritis, and transverse myelitis. Airway compromise may result from tonsillar hypertrophy; treat- ment may include steroids.

Levothyroxine accelerates the degradation of vitamin K–dependent clotting factors 20mg levitra soft. If thyroid hormone replacement therapy is started in a patient taking warfarin levitra soft 20 mg, the dosage of warfarin may need to be reduced levitra soft 20mg. Thyroid hormones increase cardiac responsiveness to catecholamines 20 mg levitra soft, thereby increasing the risk for catecholamine-induced dysrhythmias . Caution must be exercised when administering catecholamines to patients receiving levothyroxine and other thyroid preparations . Other Interactions Levothyroxine can increase requirements for insulin and digoxin . When converting patients from a hypothyroid to a euthyroid state , dosages of insulin and digoxin may need to be increased . Levothyroxine has a narrow therapeutic range , so tight control of plasma drug levels is important. To maintain good control, all pills a patient takes must produce the same levothyroxine levels. Accordingly, if a patient switches from one product to another, the new product must be bioequivalent to the old one. Whether or not any levothyroxine products—brand-name or generic—are truly equivalent is a point of contention. Hence, when blood levels of levothyroxine were measured, the values reflected the sum of endogenous thyroxine plus levothyroxine contributed by the drug— making it impossible to state with precision how much of the total was truly due to the drug. As a result, conclusions regarding the equivalence of levothyroxine products are questionable. Nonetheless, pharmacists may switch patients from one product to another, often without the knowledge of the patient or prescriber —a practice with the potential for causing toxicity or therapeutic failure. Given the debate about whether certain levothyroxine products are clinically interchangeable, what should the clinician do? Dosage and Administration I: General Considerations Routes of Administration Levothyroxine is almost always administered by mouth. Oral doses should be taken once daily on an empty stomach (to enhance absorption). Intravenous administration is used for myxedema coma and for patients who cannot take levothyroxine orally. Evaluation The goal of replacement therapy is to provide a dosage that compensates precisely for the existing thyroid deficit. This dosage is determined using a combination of clinical judgment and laboratory tests. When therapy is successful in adults, clinical evaluation should reveal a reversal of the signs and symptoms of thyroid deficiency—and an absence of signs of thyroid excess. Successful therapy of infants is reflected in normalization of intellectual function and normalization of growth and development. Duration of Therapy For most hypothyroid patients, replacement therapy must be continued for life. In addition, they should be forewarned that, although therapy will cause symptoms to improve, these improvements do not constitute a reason to interrupt or discontinue drug use. Most patients younger than 50 years can be started on full replacement doses (100–125 mcg/day for a 70-kg adult). For older adults with coronary heart disease, the starting dosage is even lower—between 12. Myxedema Coma Myxedema coma is a rare but serious condition that requires rapid treatment. Congenital Hypothyroidism In congenital hypothyroidism, thyroid hormone dosage decreases with age. For infants younger than 3 months, the dosage is 10 to 15 mcg/kg/day; for children aged 3 to 5 months, 8 to 10 mcg/kg/day; for children aged 6 to 11 months, 6 to 8 mcg/kg/day; for children aged 1 to 5 years, 5 to 6 mcg/kg/day; and for children aged 6 to 12 years, 4 to 5 mcg/kg/day. For many patients, this can be achieved with 100 to 200 mcg of levothyroxine daily. Liothyronine (T ) 3 Liothyronine [Cytomel] is a synthetic preparation of triiodothyronine, a naturally occurring thyroid hormone. Because liothyronine is the active form of levothyroxine, the3 effects of the two drugs are identical. Contrasts With Levothyroxine Liothyronine differs from levothyroxine in three important ways: (1) liothyronine has a shorter half-life and shorter duration of action, (2) liothyronine has a more rapid onset, and (3) liothyronine is more expensive. Because of its high price and relatively brief duration of action, liothyronine is less desirable than levothyroxine for long-term use. However, because its effects develop quickly, liothyronine may be superior to levothyroxine in situations that require speedy results, especially myxedema coma. Evaluation As with levothyroxine, the dosage of liothyronine is adjusted on the basis of clinical evaluation and laboratory data. Because of its short half-life, oral liothyronine is taken twice daily, in contrast to levothyroxine, which is taken once daily. Other Thyroid Preparations Liotrix Liotrix [Thyrolar] is a mixture of synthetic T plus synthetic T in a 4 : 1 fixed4 3 ratio. However, because levothyroxine alone3 produces the same ratio of T to T, liotrix offers no advantage over4 3 levothyroxine for most indications. Thyroid (Desiccated) Thyroid [Armour Thyroid, others] consists of desiccated animal thyroid glands. For practical purposes, thyroid is obsolete: use is limited to patients who have been taking the preparation for years. These agents can be used long term to treat hyperthyroidism or short term as preparation for subtotal thyroidectomy or therapy with radioactive iodine. Mechanism of Action Therapeutic effects result from blocking synthesis of thyroid hormones. First, methimazole prevents the oxidation of iodide, thereby inhibiting incorporation of iodine into tyrosine. Both effects result from inhibiting peroxidase, the enzyme that catalyzes both reactions. Please note that, although methimazole prevents thyroid hormone synthesis, it does not destroy existing stores of thyroid hormone. Hence, after therapy has begun, it may take 3 to 12 weeks to produce a euthyroid state. Therapeutic Uses Methimazole has four applications in hyperthyroidism: • It can be used as the sole form of therapy for Graves disease. Adverse Effects Methimazole is generally well tolerated but should be avoided by women who are pregnant or breastfeeding. The reaction is rare (about 3 cases per 10,000 patients) and usually develops during the first 2 months of therapy. Sore throat and fever may be the earliest indications, and patients should be instructed to report these immediately. Because agranulocytosis often develops rapidly, periodic blood counts cannot guarantee early detection. Treatment with granulocyte colony-stimulating factor (filgrastim [Neupogen]) may accelerate recovery. When given in high doses, methimazole can convert the patient from a hyperthyroid state to a hypothyroid state. Methimazole can cause neonatal hypothyroidism, goiter, and even congenital hypothyroidism. Methimazole therapy does not affect thyroid function or intellectual development in breastfed infants with doses up to 20 mg daily. Preparations, Dosage, and Administration Methimazole is supplied in tablets (5, 10, 15, and 20 mg) for oral dosing. When methimazole is discontinued, some 30% to 40% of patients remain euthyroid, indicating remission. Nonetheless, severe adverse effects can occur, especially liver injury and agranulocytosis. Treatment of Graves Disease High doses (100–300 mg 3 times a day) are used initially. Children/adolescents Thyroid hormone preparations are used in children and adolescents. Breastfeeding Thyroid hormone preparations and antithyroid medications are generally safe in breastfeeding women women. Thyroid hormone preparations and antithyroid medications can be used successfully to treat thyroid dysfunction in the older adult. Radioactive Iodine Physical Properties 131 Iodine-131 ( I) is a radioactive isotope of stable iodine that emits a combination 131 of beta particles and gamma rays. Hence, after 56 days (seven half-lives), less than 1% of 131 the radioactivity in a dose of I remains. Use in Graves Disease 131 I can be used to destroy thyroid tissue in patients with hyperthyroidism. The objective is to produce clinical remission without causing complete destruction of the gland. Unfortunately, delayed hypothyroidism, due to excessive thyroid damage, is a frequent complication. Effect on the Thyroid 131 Like stable iodine, I is concentrated in the thyroid gland. Destruction of thyroid tissue is produced primarily by emission of beta particles. About 66% of 131 patients with Graves disease are cured with a single exposure to I. First, the effect of treatment is delayed, taking several months to become maximal. Second, and more important, treatment is associated with a significant incidence of delayed hypothyroidism. Hypothyroidism results from excessive dosage and occurs in up 131 to 90% of patients within the first year after I exposure. Who Should Be Treated and Who Should Not 131 I is indicated for adults with hyperthyroidism, as well as patients who have not responded adequately to antithyroid drugs or to subtotal thyroidectomy. Also, there is 131 concern that administration of I to young patients may carry a slight risk for 131 cancer. It should be noted, however, that there is no evidence that the use of I in Graves disease has ever caused cancer of the thyroid or any other tissue. Exposure of the fetus to I after the first trimester may damage the immature thyroid, and exposure to radiation at any point in fetal life carries a risk for generalized developmental 131 harm. Dosage 131 Dosage of I is determined by thyroid size and by the rate of thyroidal iodine uptake. However, because most forms of thyroid cancer do not accumulate iodine, only a small percentage of patients 131 are candidates for I therapy. Because high amounts of radioactivity are involved, body wastes must be disposed of properly. Diagnostic Use 131 I is employed to diagnose a variety of thyroid disorders, including 131 hyperthyroidism, hypothyroidism, and goiter. After I administration, the 131 thyroid is scanned for uptake of radioactivity; the amount and location of I uptake reveal the extent of thyroid activity. Doses for diagnosis are minuscule (less than 1 microcurie for children and less than 10 microcuries for adults). Please note that, although 131 123 I can be used for diagnosis, the preferred isotope is I. Nonradioactive Iodine: Lugol Solution Description Lugol solution, also known as strong iodine solution, is a mixture containing 5% elemental iodine and 10% potassium iodide. Mechanism of Action When present in high concentrations, iodide has a paradoxical suppressant effect on the thyroid. Second, high concentrations of iodide inhibit thyroid hormone synthesis by suppressing both the iodination of tyrosine and the coupling of iodinated tyrosine residues. Third, high concentrations of iodine inhibit release of thyroid hormone into the blood. Therapeutic Use Strong iodine solution can be given to hyperthyroid individuals to suppress thyroid function in preparation for thyroidectomy. In most cases, plasma levels of thyroid hormone are reduced with methimazole before initiating strong iodine solution. In addition to its use before thyroidectomy, strong iodine solution is employed in thyrotoxic crisis. Signs and symptoms include a brassy taste, a burning sensation in the mouth and throat, soreness of the teeth and gums, frontal headache, coryza (nasal inflammation and sneezing), salivation, and various skin eruptions. Treatment consists of gastric lavage (to remove iodine from the stomach) and giving sodium thiosulfate (to reduce iodine to iodide). Dosage and Administration When employed to prepare hyperthyroid patients for thyroidectomy, strong iodine solution is administered in a dosage of 5 to 7 drops 3 times daily for 10 days immediately preceding surgery. Iodine solution should be mixed with juice or some other beverage to mask its unpleasant taste. Beta Blockers Propranolol and other beta blockers can suppress tachycardia and other symptoms of Graves disease. Benefits derive from beta-adrenergic blockade, not from reducing levels of T or T. We begin this chapter with a discussion of how estrogens and progestins regulate physiologic processes. Estrogens and progestins (also known as progestogens) are hormones with multiple actions.

In addition levitra soft 20mg, vitamin C has antioxidant activity and facilitates absorption of dietary iron levitra soft 20 mg. Sources The main dietary sources of ascorbic acid are citrus fruits and juices 20mg levitra soft, tomatoes 20 mg levitra soft, potatoes , strawberries , melons , spinach , and broccoli . Deficiency Deficiency of vitamin C can lead to scurvy , a disease rarely seen in the United States. Symptoms include faulty bone and tooth development, loosening of the teeth, gingivitis, bleeding gums, poor wound healing, hemorrhage into muscles and joints, and ecchymoses (skin discoloration caused by leakage of blood into subcutaneous tissues). Many of these symptoms result from disruption of the intercellular matrix of capillaries and other tissues. Therapeutic Use The only established indication for vitamin C is prevention and treatment of scurvy. Vitamin C has been advocated for therapy of many conditions unrelated to deficiency, including cancers, asthma, osteoporosis, and the common cold. Claims of efficacy for several of these conditions have been definitively disproved. Studies have shown that large doses of vitamin C do not reduce the incidence of colds, although the intensity or duration of illness may be decreased slightly. Research has failed to show any benefit of vitamin C therapy for patients with advanced cancer, atherosclerosis, or schizophrenia. Preparations and Routes of Administration Vitamin C is available in formulations for oral and parenteral administration. Oral products include tablets (ranging from 25–1000 mg), timed-release capsules (500−1500 mg), and syrups (20 and 100 mg/mL), as well as granules, crystals, powders, effervescent powders, and wafers. In its medicinal role, niacin is used to reduce cholesterol levels; the doses required are much higher than those used to correct or prevent nutritional deficiency. Sources Nicotinic acid (or its nutritional equivalent, nicotinamide) is present in many foods of plant and animal origin. Particularly rich sources are liver, poultry, fish, potatoes, peanuts, cereal bran, and cereal germ. Deficiency The syndrome caused by niacin deficiency is called pellagra, a term that is a condensation of the Italian words pelle agra, meaning “rough skin. When taken in large doses, nicotinic acid can cause vasodilation with resultant flushing, dizziness, and nausea. Nicotinamide, a compound that can substitute for nicotinic acid in the treatment of pellagra, is not a vasodilator, and this does not produce the adverse effects associated with large doses of nicotinic acid. Accordingly, nicotinamide is often preferred to nicotinic acid for treating pellagra. Therapeutic Uses In its capacity as a vitamin, nicotinic acid is indicated only for the prevention or treatment of niacin deficiency. Preparations, Dosage, and Administration Nicotinic acid (niacin) is available in immediate-release tablets (50–500 mg), extended-release tablets (250–1000 mg), and extended-release capsules (250– 500 mg). For treatment of pellagra, daily doses may be as high as 500 mg/day; however, the usual dose is 50-100 mg every 6-8 hours. Once major signs and symptoms have resolved, dosing can be decreased to 10 mg every 8-12 hours until resolution of skin lesions. Unlike nicotinic acid, nicotinamide has no effect on plasma lipoproteins and hence is not used to treat hyperlipidemias. Riboflavin (Vitamin B ) 2 Actions Riboflavin participates in numerous enzymatic reactions. Sources and Requirements In the United States most dietary riboflavin comes from milk, yogurt, cheese, bread products, and fortified cereals. Use in Riboflavin Deficiency Riboflavin is indicated only for prevention and correction of riboflavin deficiency, which usually occurs in conjunction with deficiency of other B vitamins. In its early state, riboflavin deficiency manifests as sore throat and angular stomatitis (cracks in the skin at the corners of the mouth). Later symptoms include cheilosis (painful cracks in the lips), glossitis (inflammation of the tongue), vascularization of the cornea, and itchy dermatitis of the scrotum or vulva. Use in Migraine Headache As discussed in Chapter 23, riboflavin can help prevent migraine headaches; however, prophylactic effects do not develop until after 3 months of treatment. Thiamine (Vitamin B ) 1 Actions and Requirements The active form of thiamine (thiamine pyrophosphate) is an essential coenzyme for carbohydrate metabolism. Thiamine requirements are related to caloric intake and are greatest when carbohydrates are the primary source of calories. As indicated, thiamine requirements increase significantly during pregnancy and lactation. Sources In the United States the principal dietary sources of thiamine are enriched, fortified, or whole-grain products, especially breads and ready-to-eat cereals. Deficiency Severe thiamine deficiency produces beriberi, a disorder having two distinct forms: wet beriberi and dry beriberi. Wet beriberi is so named because its primary symptom is fluid accumulation in the legs. Cardiovascular complications (palpitations, electrocardiogram abnormalities, high-output heart failure) are common and may progress rapidly to circulatory collapse and death. In the United States thiamine deficiency occurs most commonly among people with chronic alcohol consumption. In this population, deficiency manifests as Wernicke-Korsakoff syndrome rather than frank beriberi. This syndrome is a serious disorder of the central nervous system, having neurologic and psychological manifestations. Symptoms include nystagmus, diplopia, ataxia, and an inability to remember the recent past. Accordingly, if Wernicke-Korsakoff syndrome is suspected, parenteral thiamine should be administered immediately. Therapeutic Use The only indication for thiamine is treatment and prevention of thiamine deficiency. Parenteral administration is reserved for severe deficiency states (wet or dry beriberi, Wernicke-Korsakoff syndrome). The dosage for beriberi is 5 to 30 mg/day orally in single or divided doses 3 times/day for 1 month. Pyridoxine (Vitamin B ) 6 Actions Pyridoxine functions as a coenzyme in the metabolism of amino acids and proteins. However, before it can do so, pyridoxine must first be converted to its active form: pyridoxal phosphate. Sources In the United States the principal dietary sources of pyridoxine are fortified, ready-to-eat cereals; meat, fish, and poultry; white potatoes and other starchy vegetables; and noncitrus fruits. Deficiency Pyridoxine deficiency may result from poor diet, isoniazid therapy for tuberculosis, and inborn errors of metabolism. Symptoms include seborrheic dermatitis, anemia, peripheral neuritis, convulsions, depression, and confusion. In the United States dietary deficiency of vitamin B is rare, except among6 people who abuse alcohol on a long-term basis. Within this population, vitamin B deficiency is estimated at 20% to 30% and occurs in combination with6 deficiency of other B vitamins. Isoniazid (a drug for tuberculosis) prevents conversion of vitamin B to its6 active form and may thereby induce symptoms of deficiency (peripheral neuritis). Inborn errors of metabolism can prevent efficient utilization of vitamin B,6 resulting in greatly increased pyridoxine requirements. Unless treatment with vitamin B is initiated early, permanent cognitive deficits may result. Drug Interactions Vitamin B interferes with the utilization of levodopa, a drug for Parkinson6 disease. Accordingly, patients receiving levodopa should be advised against taking the vitamin. Therapeutic Uses Pyridoxine is indicated for prevention and treatment of all vitamin B deficiency6 states (dietary deficiency, isoniazid-induced deficiency, pyridoxine dependency syndrome). Preparations, Dosage, and Administration Pyridoxine is available in solution (200 mg/5 mL), standard tablets (25, 50, 100, 250, and 500 mg), extended-release tablets (200 mg), and capsules (150 mg) for oral use. To correct dietary deficiency, the dosage is 10 to 20 mg/day for 3 weeks followed by 1. To protect against developing isoniazid- induced deficiency, the dosage is 25 to 50 mg/day. Pyridoxine dependency syndrome may require initial doses up to 600 mg/day followed by 25 to 50 mg/day for life. Because deficiency presents as anemia, folic acid and cyanocobalamin are discussed in Chapter 45. Because adults older than 50 years often have difficulty absorbing dietary vitamin B12, they should ingest at least 2. Food Folate Versus Synthetic Folate The form of folate that occurs naturally (food folate) has a different chemical structure than synthetic folate (pteroylglutamic acid). As a result of grain fortification, the incidence of folic acid deficiency in the United States has declined dramatically. Unfortunately, the incidence of birth defects from folate deficiency (see later) has only dropped by 32%. Spina bifida, a condition characterized by defective development of the bony encasement of the spinal cord, can result in nerve damage, paralysis, and other complications. Folic Acid and Cancer Risk There is evidence that folic acid in low doses may reduce cancer risk, whereas folic acid in higher doses may increase cancer risk—suggesting that cancer risk is increased by having either too little folic acid (folic acid deficiency) or by having too much folic acid (folic acid excess). Taking high- dose folic acid to reduce cancer risk is ineffective and should be discouraged. Pantothenic Acid Pantothenic acid is an essential component of two biologically important molecules: coenzyme A and acyl carrier protein. Coenzyme A is an essential factor in multiple biochemical processes, including gluconeogenesis, intermediary metabolism of carbohydrates, and biosynthesis of steroid hormones, porphyrins, and acetylcholine. Pantothenic acid is available in single-ingredient tablets and in multivitamin preparations. However, because deficiency does not occur, there is no reason to take supplements. Biotin Biotin is an essential cofactor for several reactions involved in the metabolism of carbohydrates and fats. The vitamin is found in a wide variety of foods, although the exact amount in most foods has not been determined. In addition to being available in foods, biotin is synthesized by intestinal bacteria. In fact, to determine the effects of deficiency, scientists had to induce it experimentally. When this was done, subjects experienced dermatitis, conjunctivitis, hair loss, muscle pain, peripheral paresthesias, and psychological effects (lethargy, hallucinations, depression). Biotin appears devoid of toxicity: subjects given large doses experienced no adverse effects. Excessive body fat may be associated with increased risk for morbidity from hypertension, coronary heart disease, ischemic stroke, type 2 diabetes, gallbladder disease, liver disease, kidney stones, osteoarthritis, sleep apnea, dementia, and certain cancers. Among women, obesity may increase the risk for menstrual irregularities, amenorrhea, and polycystic ovary syndrome. During pregnancy, obesity may increase the risk for morbidity and mortality for both mother and child. Despite recent declines in obesity prevalence, almost one third of American children and adolescents are overweight or obese. In addition, type 2 diabetes, formerly seen almost exclusively in adults, has increased 10-fold among children and teens, and gallbladder disease has tripled. Contributing factors include genetics, metabolism, and appetite regulation, along with environmental, psychosocial, and cultural factors. Although obese people can lose weight, the tendency to regain weight cannot be eliminated. Assessment of Weight-Related Health Risk Health risk is determined by (1) the degree of obesity (as reflected in the body mass index), (2) the pattern of fat distribution (as reflected in the waist circumference measurement), and (3) the presence of obesity-related diseases or cardiovascular risk factors. Accordingly, all three factors must be assessed when establishing a treatment plan. Nor do they apply to competitive athletes or bodybuilders, who are heavy because of muscle mass rather than excess fat. Accumulation of fat in the upper body, and especially within the abdominal cavity, poses a greater risk to health than does accumulation of fat in the lower body (hips and thighs). People with too much abdominal fat are at increased risk for insulin resistance, diabetes, hypertension, coronary atherosclerosis, ischemic stroke, and dementia. Fat distribution can be estimated simply by looking in the mirror: an apple shape indicates too much abdominal fat, whereas a pear shape indicates fat on the hips and thighs. Certain weight-related diseases—established coronary heart disease, other atherosclerotic diseases, type 2 diabetes, and sleep apnea—confer a risk for complications and mortality. Other weight-related diseases—gynecologic abnormalities, osteoarthritis, gallstones, and stress incontinence—confer less risk. The risk is further increased by weight-related diseases and cardiovascular risk factors. Overview of Obesity Treatment The strategy for losing weight is simple: take in fewer calories per day than are burned. After 6 months, the goal for all patients is to prevent lost weight from returning. This may be accomplished by a combination of diet, physical activity, and behavioral therapy. A more realistic goal is to target a percentage of body weight at which risk is decreased and comorbidities prevented. A weight loss of 10% to 15% is typical for those who diligently adhere to medication and lifestyle regimen, whereas a loss greater than 15% is exceptional. Treatment Modalities Weight loss can be accomplished with five treatment modalities: caloric restriction, physical activity, behavioral therapy, drug therapy, and surgery.

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